One of the holy grails of cancer research is to identify tumors that need to be aggressively treated. For prostate cancer, for example, after decades of intensive research, there is still no prognostic marker to distinguish between indolent and aggressive tumors. There is no reliable way to identify which tumors need to be treated aggressively and which do not need aggressive treatment. Therefore, the importance of finding a clinically relevant prognostic marker for prostate cancer cannot be over-estimated.
TMPRSS2-ERG fusion, caused by a chromosomal translocation, occurs in ˜50% of primary prostate tumors and results in over-expression of a truncated but functional erythroblast transformation-specific (ETS)-related gene (ERG) in prostate tumors. It is believed that oncogenic ERG is the driver of prostate tumorigenesis. ERG is a member of the ETS family of transcription factors. It contains an ETS DNA-binding domain and can directly regulate target gene expression. However, the inventors reasoned that, as a transcription factor, ERG per se does not cause tumorigenesis. Instead, the downstream genes that are activated (or suppressed) by ERG in the human prostate could have contributed to prostate cancer development. Similarly, as a transcription factor, p53 exerts its tumor suppressor function mainly through its downstream transcriptional products, such as p21 and Bax.
The present disclosure utilizes ERG targets, in certain embodiments, to satisfy a long-felt need in the art to provide means to determine prognosis, diagnosis, and/or treatment regimens for cancer, such as for prostate cancer.